Dietary ingestion of the creatine analogue cyclocreatine (1-carboxymethyl-2-iminoimidazolidine, CCr) imparts to tissue the ability to sustain high levels of myocardial adenosine triphosphate (ATP), or at least to delay the depletion of ATP during total ischemia. Cyclocreatine is reported to be effective provided the dietary supplement is ingested over a period of at least two days prior to the onset of ischemia; but a maximum response is achieved where the dietary supplement has been provided over a period of about ten to fourteen days prior to onset of ischemia. This period of time can be required in order to permit the dietary supplement, cyclocreatine, to undergo phosphorylation (to form cyclocreatine phosphate, 1-carboxymethyl-2-imino-3-phosphono-imidazolidine, CCrP). This synthetic phosphagen is believed to be effective in helping to conserve the total adenylate pool and to buffer the decrease in the ratio of ATP to free adenosine diphosphate (ADP) that results from ischemia. Dietary ingestion of cyclocreatine also delays the development of acidosis and the onset of poor ventricular compliance, as evidenced by a rigor-like increase in tonic pressure, during ischemia.